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Regulation of Fc receptor and major histocompatibility complex antigen expression on isolated rat microglia by tumour necrosis factor interleukin-1 and lipopolysaccharide: effects on interferon-gamma induced activation.

机译:肿瘤坏死因子白介素-1和脂多糖对离体大鼠小胶质细胞的Fc受体和主要组织相容性复合物抗原表达的调节:对干扰素-γ诱导的激活的影响。

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摘要

Isolated rat brain microglia display enhanced expression of Fc receptors on treatment with interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and lipopolysaccharide (LPS), whereas major histocompatibility complex (MHC) antigen expression is enhanced only by IFN-gamma. Although TNF and LPS individually have no effect on MHC expression by microglia, they both antagonize IFN-gamma-induced expression. The enhanced expression of Fc receptors observed in the presence of IFN-gamma, TNF or LPS is significantly inhibited by the combination of IFN-gamma with either LPS or TNF. IL-1 alpha has little effect on IFN-gamma-induced MHC or Fc receptor expression by microglia. Peritoneal macrophages behave similarly to microglia, with the notable exception that IL-1 alpha enhances IFN-gamma-induced FcR expression. These observations suggest that the functional activity of microglia during inflammation or demyelination in the central nervous system can be influenced by the changing profile of cytokines present during lesion development.
机译:分离的大鼠脑小胶质细胞在干扰素-γ(IFN-γ),肿瘤坏死因子-α(TNF-α),白介素-1(IL-1)和脂多糖(LPS)的治疗下显示出增强的Fc受体表达,而主要组织相容性复合体(MHC)抗原表达仅通过IFN-γ增强。尽管TNF和LPS分别对小胶质细胞的MHC表达没有影响,但它们都拮抗IFN-γ诱导的表达。在IFN-γ,TNF或LPS存在下观察到的Fc受体表达的增强被IFN-γ与LPS或TNF的组合显着抑制。 IL-1α对小胶质细胞对IFN-γ诱导的MHC或Fc受体表达影响很小。腹膜巨噬细胞的行为类似于小胶质细胞,但值得注意的例外是IL-1α增强了IFN-γ诱导的FcR表达。这些观察结果表明,小胶质细胞在中枢神经系统炎症或脱髓鞘过​​程中的功能活性可能受到病变发展过程中细胞因子变化的影响。

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